Showing papers on "Fetus published in 1980"

Echocardiographic Studies of the Human Fetus: Prenatal Diagnosis of Congenital Heart Disease and Cardiac Dysrhythmias

Abstract: During obstetrical ultrasound examinations, 200 M-mode and 35 real-time two-dimensional echocardiographic studies were performed on 180 fetuses of high-risk pregnancies. Fetal gestational ages ranged from 18 to 41 weeks. M-mode "sweeps" demonstrating mitral- and septal-aortic fibrous continuity were obtained in 115 studies. Paradoxic septal motion in 50 fetuses suggested relarive right ventricular volume loading. Congenital cardiac malformations were accurately diagnosed in a 34-week fetus with pulmonary atresia and hypoplastic right ventricle and in a 28-week fetus with a univentricular heart. Congenital complete atrioventricular block was diagnosed in a 28-week fetus and atrial flutter with variable atrioventricular block was diagnosed in a 38-week fetus. The use of echocardiographic studies to evaluate cardiac structure and rhythm in utero assists in counseling prospective parents and in planning postnatal management for their offspring.

Sex Steroids in the Umbilical Circulation of Fetal Rhesus Monkeys from the Time of Gonadal Differentiation

Abstract: Male rhesus monkey fetuses have significantly more testosterone (T) in their circulation than females on days 35–50 of gestation (P < 0.01; n = 6 males and 6 females). However, we found no sex differences for androstenedione (Δ4). T concentrations remained significantly higher in male fetuses than in females later in gestation, e.g. days 79–84, 100–133, and 140–160. Levels of Δ4 differed between the sexes only on days 79–84, and dihydrotestosterone concentrations were significantly higher in male fetuses than in females on days 100–133 and 140–163. The fact that Δ4 concentrations were not different betweenthe sexes at the earliest period studied (days 35–50) indicatesthat systemic concentrations of this hormone in the fetus probably are not important for sexual differentiation, especially of the central nervous system. Quantification of three steroids (T,Δ, and dihydrotestosterone) in umbilical arterial and venous plasma from five male and nine female fetuses (days 35–100) revealed significant arterial/ve...

Bovine virus diarrhoea-mucosal disease virus: pathogenicity for the fetal calf following maternal infection.

Abstract: Fifteen pregnant, bovine virus diarrhoea-mucosal disease (BVD-MD) antibody-free Jersey heifers were infected experimentally with a mixture of 10 cytopathic strains of BVD-MD virus isolated from cattle in Britain. Each cow was inoculated intramuscularly on gestation day 100 with a high or a low dose of virus grown in primary calf testis tissue cultures. None of the cows showed clinical signs of illness following exposure, but all had seroconverted within six weeks. Six fetuses, including one set of twins, died in utero following infection. Of these five were aborted between days 136 and 154; the sixth one was mummified and still retained at day 300. The remaining 10 fetuses survived to term, but all showed evidence of intrauterine growth retardation with or without gross malformation and/or dysmyelination of the central nervous system. Three were clinically affected with congenital nervous disease. Of the 10 liveborn fetuses, two had specific serum antibodies to BVD-MD. Non-cytopathic BVD-MD virus was recovered from all of the remaining eight. When non-immune cows become infected with BVD-MD virus in mid gestation: transplacental infection of the fetus will probably result; apart from the risk of fetal death, with or without abortion, there is a high probability of fetal mal-development which may not always be clinically obvious; the immunological competence of the fetus may be impaired; congenital infection is likely in a substantial proportion of liveborn calves. About one in 16 bovine fetuses in British herds are estimated to be at risk from BVD-MD virus infection.

Effects of epidermal growth factor on lung maturation in fetal lambs.

Abstract: Summary Injection of epidermal growth factor (EGF) into 24-day rabbit fetuses (5 pg, im or ip) induced accelerated maturation of the lung. On sacrifice at day 27, there was greater distensibility and stability on deflation associated with the appearance of a complement of type I1 cells approaching that of the rabbit at term. EGF treatment had no demonstrable effect on body weight or lung weight in this group of animals. Saline-injected control fetuses were not affected significantly. Speculation EGF is capable not only of promoting epithelial cell growth but also differentiation in the fetal rabbit lung. It may be an important hormone in the maturation of the lung and capable of protecting the prematurely delivered fetus against the development of hyaline membrane disease. EGF is a biologically active polypeptide first described in 1962 by Cohen (6), who observed that the daily injection of an extract of male mouse submaxillary gland into immature mice resulted in precocious tooth eruption and eye opening. Subsequent analysis of the salivary gland extract revealed that the biologically active component was a heat-stable, nondialyzable, single polypeptide chain of 53 amino acid residues with a molecular weight of 6045 daltons, as determined by amino acid composition (21). The biologic effects of EGF have been shown to be primarily those of generalized epithelial growth and keratinization. These effects of mouse-derived EGF (mEGF) have been demonstrated not only in the mouse and rat, but also in other species such as cultured chick embryo skin (7), human fibroblasts (8), and both chick and human embryo cornea (18). Recently, it has been demonstrated that EGF is also present in the human and that human EGF, when tested in organ culture systems, appeared to act in a manner identical to that of mEGF (19). In 1975. it was proposed that if EGF is a normal fetal growth hormone, it mig& aiso be capable of stimulating pulkonary e~ithelial cell growth. It was shown that the constant infusion of

Utilization of substrates by the ovine placenta in vivo.

Abstract: The uptakes of oxygen, glucose, and amino acids by the pregnant uterus via the uterine circulation and by the fetus via the umbilical circulation have been measured in sheep during the last month of gestation. The umbilical uptakes of oxygen and glucose are approximately 55 and 28%, respectively, of the total uterine uptake. This discrepancy between uterine and umbilical uptakes is due primarily to a large utilization rate of oxygen and glucose by the placenta. Part of the placental utilization of glucose can be accounted for by placental lactate excretion into both maternal and fetal blood. In marked contrast to the pattern of glucose utilization, the comparison of uterine and umbilical amino acid uptakes shows that the bulk of the amino acids taken up by the pregnant uterus is transferred to the fetus. The placenta utilizes glutamate of fetal origin and produces ammonia, which is excreted primarily into the maternal circulation.

Glucocorticoids increase pulmonary s-adrenergic receptors in fetal rabbit

Abstract: beta-Adrenergic agonists stimulate surfactant release and decrease fluid in lung alveoli of fetuses. Both effects are most evident toward the end of gestation. We used [3H] dihydroalprenolol (DHA) to investigate the development of pulmonary beta-adrenergic receptors in rabbit fetuses and to study the effect of glucocorticoid treatment on the beta-receptor number. In the lung particulate preparation, DHA binding was rapid, reversible, stereoselective, and of high affinity. The order of potency for adrenergic agonists in competing for DHA binding was isoproterenol > epinephrine = norepinephrine, which is typical of interactions at a beta 1-adrenergic receptor. Using DHA, we demonstrated that the concentration of pulmonary beta-receptors increased significantly between 28 and 31 days of gestation; however, there was no change in the dissociation constant during gestation. After injecting betamethasone (0.17 mg/kg, 24 hours) into rabbits at 25 days of pregnancy, we found that the concentration of pulmonary beta-receptors increased from 44.2 +/- 6.6 fmol/mg protein in untreated fetuses to 77.9 +/- 5.6 fmol/mg protein in treated fetuses. However, this treatment did not affect the DHA binding sites in the fetal rabbit heart. Maternal treatment with the T3 analogue 3,5-dimethyl-3'-isopropyl-L-thyronine (0.5-1 mg/kg) at a dosage which increased both surfactant synthesis and release did not alter pulmonary receptor concentration. Our results indicate that the concentration of pulmonary beta-adrenergic receptors increases in the fetus at term and suggest that this increase is stimulated by endogenous glucocorticoid in fetal circulation.

Effects of a sustained insulin infusion upon glucose uptake and oxygenation of the ovine fetus.

Abstract: Summary: The effect of insulin upon fetal metabolism is an important question to resolve, bearing in mind that the metabolic effects of insulin on the fetus could differ both quantitatively and qualitatively depending upon the degree and duration of the hyperinsulinemia. The present study was designed to determine whether the effect of fetal hyperinsulinemia on umbilical glucose uptake could be sustained over several days of infusion with various levels of insulin. An unexpected outcome of the study was the observation that this procedure was accompanied by the development of fetal hypoxia. Fetal glucose/oxygen quotients (G/O2) increased during fetal insulin infusions from a mean of 0.48 during the control period to 0.71 when fetal insulin levels were less than 80 micro units/ml (P < 0.01) and to 0.85 when fetal insulin levels were greater than 200 micro units/ml (P < 0.001). The increase in G/O2 occurred within 4 hr of infusion in all cases (P < 0.005) and was sustained for the duration of the infusions. The increase in G/O2 was due to a significant rise in the arteriovenous differences of whole blood glucose across the umbilical circulation (P < 0.001). Oxygen content differences across the umbilical circulation also increased during infusion (P < 0.005). This was due primarily to a significant and progressive decline in the fetal arterial oxygen content (P < 0.001). By 24 hr after the insulin had been stopped, the oxygen content rose and returned to pre-infusion values by the 3rd day of recovery. Fetal plasma glucose concentration fell during insulin infusion (P < 0.001) and rebounded sharply to levels significantly higher than control values (P < 0.001) within 4 hr after the infusion was stopped. The plasma glucose returned to control values by the 3rd day of recovery. Insulin levels ranged from 0–16 micro units/ml during control periods and from 48–1166 micro units/ml during infusion. There was a significant positive correlation between the G/O2 quotient and the log of fetal insulin concentration. There was a negative correlation between the fetal arterial oxygen content and insulin concentration. Five twin pairs were studied in which one twin served as control and the other as the infusion subject. The values of glucose, G/ O2, and arteriovenous differences of glucose and oxygen were significantly different between the infused and control twin fetuses within 4 hr of infusion and the oxygen content was significantly lower in the infused twin by 24 hr of infusion. There were no significant differences in these measurements between the twins before infusion. Speculation: Insulin infusions of several days duration into the fetal lamb cause a sustained increase in umbilical glucose uptake and a decrease in fetal arterial oxygen content. The progressive decline in fetal arterial oxygen content during infusion may be due to an increase in fetal oxygen consumption. The effect of insulin upon fetal oxygenation may be one of the pathophysiologic factors contributing to the increased intrauterine death rate of infants of diabetic mothers.

Qualitative real-time cross-sectional echocardiographic imaging of the human fetus during the second half of pregnancy.

Abstract: In this study, we used high-resolution echocardiographic systems to investigate how early in pregnancy normal fetal cardiac anatomy could be noninvasively evaluated. Over a 2-year period, 84 of 88 fetuses were successfully imaged (27 were studied serially). Postnatal images of 73 were obtained during the newborn period. Estimated fetal age varied at initial examination from 19-41 weeks (mean +/- 0.5 weeks [+/- SEM]) of pregnancy. Estimated fetal weight using an ultrasound algorithm varied from 500-3100 g (mean 1580 +/- 80 g [+/- SEM]). To evaluate fetal cardiac anatomy, we reproduced commonly used cross-sectional views of the heart. The four-chamber and the short-axis great artery views have been most successful for cardiac evaluation in the fetus. These views could be obtained in 96% and 95% of the patients, respectively. With these views, cardiac chamber and valve structures, as well as two great arteries, could be imaged in detail. The ascending and descending aorta, as well as the aortic arch and vessels to the arms and head, were visualized in 87% of examinations, and the inferior and superior venae cavae were visualized in 76%. In two of three RH fetuses, changes in cardiac chambers compatible with hydrops fetalis were demonstrated. We examined all fetuses after birth and verified clinically (or noninvasively) that no cardiac malformations were present. It appears, however, that the diagnosis of major congenital heart defects should be possible before birth.

Fetal toxicity of cadmium in the rat: Maternal vs fetal injections

Abstract: Fetal death in rats was produced by subcutaneous injections of CdCl2 (40 mumoles/kg) on day 18 of pregnancy. The incidence of fetal death following these maternal injections was 74.9%, with mean (+/- SD) fetal cadmium burdens of 8.6 +/- 4.4 nmoles. To separate maternal from fetal effects of cadmium, doses of CdCl2 up to 60 mumoles/kg fetal weight were injected directly into fetuses on day 18 of gestation. Fetal viability was then determined on gestational day 21. Following direct fetal injection, mean fetal body burdens of cadmium were 74.6 +/- 34.8 nmoles, but the incidence of fetal dealth was only 11.5%. The high incidence of fetal death following maternal exposure to CdCl2 is not solely explained by the direct effects of CdCl2 on the fetus. Thus, the fetal toxicity of cadmium may be the result of some extra-fetal mechanism such as maternal toxicity or the observed placental necrosis.

Distribution and recirculation of umbilical and systemic venous blood flow in fetal lambs during hypoxia.

Abstract: The presence of vascular shunts in the fetal circulation results in mixture of oxygenated blood returning from the placenta with venous blood returning from the fetal body. In fetal sheep with chronically implanted vascular catheters we found during normal oxygenation that 22% of umbilical venous blood recirculated to the placenta without being presented to the fetal tissues (left-to-right shunt analogue) while about half of systemic venous blood recirculated to the fetal body and not to the placenta for oxygenation (right-to-left shunt analogue). These shunts comprised 34% of cardiac output and increase the workload on the fetal heart, as they are ineffective in terms of oxygen uptake and delivery. In normally-oxygenated fetuses, 11% of cardiac output was comprised of umbilical venous blood recirculating to the placenta (left-to-right shunt analogue) whereas 23% of cardiac output consisted of systemic venous blood circulating to the fetal body (right-to-left shunt analogue). During induced maternal-fetal hypoxia (10% O2 to ewe), although the percentage of ineffective cardiac output did not change (31%), the left-to-right shunt analogue increased to 19% and the right-to-left shunt analogues decreased to 12% of cardiac output. Hypoxia also resulted in an increase in the percentage of umbilical venous blood which bypassed the liver through the ductus venosus (control 57 +/- 12%; hypoxia 65 +/- 12%, P < 0.02), causing the proportion of umbilical venous blood contributing to the fetal cardiac output to increase from 27 +/- 10% during normoxia to 39 +/- 9% during hypoxia (P < 0.005). This factor, together with the redistribution of cardiac output during hypoxia, resulted in a 100% increase in oxygen delivery from umbilical venous blood to the myocardium and a maintenance of the umbilical vein derived oxygen supplied to the brain and placenta, despite a 40% reduction in total available oxygen in umbilical venous blood.

Morphological effects of chronic bilateral phrenectomy or vagotomy in the fetal lamb lung.

Abstract: The relationship between fetal espiratory activity and fetal lung development has been studied at the cellular level using two experimental models. Chronic bilateral phrenectomy over a period of 20-28 days during the last trimester of the fetal lamb resulted in hypoplastic lungs, although cellular maturity, as indicated by the presence of alveolar epithelial Type II cells, was present. In the lungs from fetal lambs undergoing sham operations for a similar time course there was evidence of enhanced alveolar proliferation when compared with lungs from normal fetal sheep of a similar gastational age, most probably as a result of operative stress. Following chronic bilateral vagotomy no changes in size or histology of the fetal lamb lungs were detected. At an ultrastructural level, however, inclusions of Type II cells consistently showed the loss of the typical osmiophilic lamellated appearance. These results indicate the importance of the fetal breathing apparatus in maintaining a volume of lung liquid which is adequate for normal pulmonary development, particularly during the phase in which alveoli are formed.

Direct evidence of sudden rise in fetal corticoids late in human gestation.

Abstract: Glucocorticoids accelerate fetal lung maturation in all mammals studied, and in some species, such as goat and sheep, concentrations of fetal cortisol increase sharply before term, bringing about a train of events leading to parturition. Studies of cortisol in the umbilical cord blood have revealed no such increase at the end of human pregnancy. But information obtained in that way is difficult to interpret because much of the fetal cortisol is of maternal origin and its concentration, if sampled at delivery, is affected by maternal stress. These problems can be avoided to some extent by studying other fetal corticoids. Corticosterone sulphate (once called compound B, and abbreviated to BS) is produced by fetal adrenal glands and is present in greater concentrations in human fetal plasma than in maternal plasma. It is hydrolysed by the placental sulphatases and is a poor substrate for for placental 11 beta- hydroxysteroid dehydrogenase. We report here confirmation that the bulk of maternal BS originates from the fetus, and that its concentration increases suddenly at term.

Changes in the circulating form of serum somatomedin-c during fetal life

Abstract: The predominant form of somatomedin-C (Sm-C) in human postnatal serum elutes from gel chromatographic columns at an approximate molecular weight of 150,000 daltons (150 K). Nine of 10 infants of 30 weeks gestation or more had elution profiles similar to postnatal sera, while in 7 of 9 infants of 27 weeks or less, the immunoreactive Sm-C eluted predominantly at an apparent molecular weight of 40,000 daltons (40 K). Five infants between 26–32 weeks exhibited a transitional pattern. One 43 week gestation anencephalic infant exhibited only 40 K Sm-C, suggesting that the 150 K proteins which bind Sm-C are acquired in response to growth hormone or other pituitary hormones. Even though the 40 K form of Sm-C is the only form found in mid-gestation fetal serum and in media from in vitro fetal mouse liver explants, it probably does not represent the primary gene product. This is suggested by the observation that 40 K Sm-C also binds 125I-Sm-C and can be dissociated by acid and, therefore, probably is a complex of S...

High Pulmonary Vascular Resistance After Birth: I. Pathophysiologic Considerations and Etiologic Classification

Abstract: The clinical syndrome known as persistent fetal circulation, or persistent pulmonary hypertension of the newborn, is characterized by maintenance of a high pulmonary vascular resistance after birth. The small pulmonary arteries of the fetus have a thick muscular medial layer; they are very reactive, being actively constricted by the low PO2 levels normally present during fetal life. The pulmonary vascular smooth muscle layer is hypertrophied in conditions that result in chronic fetal hypoxia, or a maintained increase in pulmonary arterial pressure. Normally, pulmonary vasodilation occurs rapidly after birth, partly related to physical expansion with gas, but mainly due to the increased PO2 associated with ventilation with air. Based on these developmental considerations, the factors responsible for an increased pulmonary vascular resistance after birth may be classified in three main groups: (A) Acute vaso constriction due to postnatal hypoxia and aggravated by acidemia; (B) Prenatal increase in pulmonary...

Serum Testosterone Concentrations in Embryonic and Fetal Pigs During Sexual Differentiation

Abstract: Testosterone concentration in serum of the umbilical artery was greater for male than female fetuses at all stages sampled from Day 30 to Day 112 of gestation. For male fetuses testosterone concentrations increased from Day 30 to a maximum on Day 35 and decreased thereafter. The pattern of testosteroneconcentrations in amniotic fluidmimicked that observed in serum of the umbilical artery. The concentration of testosterone on Days 40 and 50 of gestation was three to four times greater in the umbilical artery than in the umbilical vein. These data indicate that fetal testes are secreting testosterone in vivo during differentiation of the internal and external genitalia. Serum testosterone concentrations are greater during the stage of sexual differentiation than at later stages.